Taken together, these data suggest that IL-17 and IL-22 can promote subepithelial fibrosis in asthma by a direct action on fibrocytes and fibroblasts, activating collagen production and deposition in ECM, promoting metalloprotease activity, angiogenesis and cell proliferation, enhancing Th17 response and in situ neutrophil recruitment, and inhibiting fibroblasts apoptosis. The gene discussed is IL22; the disease is asthma.